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DEFINITION

A DISTURBANCE IN CARBOHYDRATE AND VOLATILE FATTY ACIDS METABOLISM LEAD TO INTOXICATION DUE TO ACCUMULATION OF KETONE BODIES IN BLOOD
ANIMAL SUSCEPTIBILITY
THE DISEASE AFFECT MAINLY THE HIGH PRODUCING DAIRY COWS ABOUT 10 DAYS TO SIX WEEKS AFTER CALVING. ALSO THE DISEASE OCCURS MAINLY IN ANIMAL HOUSED DURING THE WINTER AND SPRING MONTHS AND RARE IN COWS THAT CALVE IN PASTURE.
ETIOLOGY
ALL EFFECTED COWS SHOW LOW BLOOD GLUCOSE CONC. NORMAL BLOOD GLUCOSE CONC. IS 50 -80 MG % ; IN KETOSIS LESS THAN 40 MG% AND 20 MG%.
1- ABSOLUTE CARBOHYDRATE DEFICIENCY ( PRIMARY).
2-RELATIVE CARBOHYDRATE DEFICIENCY ( SECONDARY).
3- DISTURBANCE IN CARBOHYDRATE METABOLISM.
A- SUDDEN CHANGE IN DIET AFTER PARTURITION FROM CARBOHYDRATE RICH TO PROTEIN RICH DIET .
B- STARVATION LEAD TO DECREASE IN PROPIONIC ACID.
C- COBALT DEFICIENCY.
D- LOSS OF EXERCISE.

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TYPES OF BOVINE KETOSIS

PRIMARY KETOSIS ( PRODUCTION KETOSIS). OCCUR IN COWS IN GOOD EXCESSIVE BODY CONDITION THAT HAVE HIGH LACTATION POTENTIAL AND ARE BEING FEED GOOD QUALITY RATION.

SECONDARY KETOSIS DUE TO THE DISEASE RESULT IN DECREASE OF FOOD INTAKE LIKE ABOMASAL DISPLACEMENT, TRP, METRITIS.

PATHOGENESIS

THE PRINCIPAL METABOLIC DISTURBANCES OBSERVED , HYPOGLYCEMIA AND KETONEMIA , MAY BOTH EXERT AN EFFECT ON THE CLINICAL SYNDROME.
IN MANY CASES , THE SEVERITY OF THE CLINICAL SYNDROME IS PROPORTIONAL TO THE DEGREE OF HYPOGLYCEMIA AND KETONEMIA .
THE NERVOUS SIGNS WHICH OCCUR DUE TO THE REQUIREMENT OF NERVOUS TISSUE FOR GLUCOSE TO MAINTAIN NORMAL FUNCTION MAY ALSO BE A FACTOR IN THESE CASES. HOWEVER THE KETONE BODIES MAY EXERT AN ADDITIONAL INFLUENCE ON THE SIGNS OBSERVED . ACETOACETIC ACID IS KNOWN TO BE TOXIC AND PROBABLY CONTRIBUTES TO THE TERMINAL COMA .
THE NERVOUS SIGNS WHICH OCCUR IN SOME CASES OF BOVINE KETOSIS ARE THOUGHT TO BE CAUSED BY PRODUCTION OF ISOPROPYL ALCOHOL , A BREAKDOWN PRODUCT OF ACETOACETIC ACID IN THE RUMEN .

CLINICAL FINDINGS

THE BOVINE KETOSIS OCCURS IN TWO FORMS :
1- WASTING FORM
GRADUAL AND MODERATE DECREASE IN APPETITE AND MILK PRODUCTION.
BODY WEIGHT IS LOST RAPIDLY LEAD TO WOODY APPEARANCE DUE TO LOSS OF COETANEOUS ELASTICITY.
TPR IS NORMAL AND RUMINAL MOVEMENT IS DECREASE IN AMPLITUDE AND NUMBER.
THE FECES ARE FIRM AND DRY BUT SERIOUS CONSTIPATION DOES NOT OCCUR.
CHARACTERISTIC ODOR OF KETONE IS DETECTABLE ON THE BREATH AND OFTEN IN MILK.
VERY FEW AFFECTED ANIMALS DIE BUT WITHOUT TREATMENT AND ALTHOUGH SPONTANEOUS RECOVERY USUALLY OCCUR OVER ABOUT MONTH.
2- NERVOUS FORM
THE SIGNS BEGIN QUITE SUDDENLY. THE SYNDROME IS SUGGESTIVE OF DELIRIUM RATHER THAN OF FRENZY THE CHARACTERISTICS SIGNS INCLUDE:
A- WALKING IN CIRCLES
B- CROSSING OF THE LEGS OR STRADDLING OF THE LEGS.
C- HEAD PUSHING IN TO THE STANCHION.
D- APPARENT BLINDNESS
E- AIMLESS MOVEMENT.

THE NERVOUS SIGNS USUALLY OCCURS IS SHORT EPISODES.

AFFECTED COW MAY INJURE THEMSELVES DURING THE NERVOUS EPISODES
DIAGNOSIS
CASE HISTORY
CLINICAL SIGNS
ESTIMATION OF BLOOD GLUCOSE LEVEL
ESTIMATION OF KETONE BODY IN BLOOD , NORMAL 10 MG /DL REACH TO 20-100 MG /DL
URINE ANALYSIS DETECT THE KETONE BODIES IN URINE LEVEL OF 80-1300 MG/DL INDICATE THE PRESENCE OF KETOSIS OR BY ROTHERA'S TEST.
MILK KETONE , NORMAL 3 MG/ DL REACH TO 40 MG /DL

◙ CLINICAL CHEMISTRY AND HEMATOLOGY

TREATMENT

A- REPLACEMENT THERAPY

GLUCOSE 50 % SOLUTION IN DOSE 500 ML FOR 5 DAYS I/V OR S/C.

B - OTHERS

PROPYLENE GLYCOL ( GLYCERIN) IN DOSE OF 225 GR TWICE DAILY FOR 2 DAYS FALLOWED BY 110 GR DAILY FOR 2 DAYS ( ORALLY).

- SODIUM PROPIONATE 110- 250 GR DAILY

- LACTATE ( CAL & SOD. LACTATE ) 1 KG INITIALLY FALLOWED BY 0.5 KG DAILY FOR 7 DAYS.

- SODIUM ACETATE 110 – 500 GR/DAY

- AMMONIUM LACTATE 200 GR DAILY FOR 5 DAYS .

C- HORMONAL THERAPY .

GLUCOCORTICODES 50 -100 IU/COW FOR 3 DAYS.

INSULIN 200-300 IU/ COW.

D- MISCELLANEOUS TREATMENT

A - VIT B12 4.7 MG/KG B.W WEEKLY FOR 3-4 WEEKS

B - COBALT SULFATE OR COBALT CHLORIDE 5 MG/COW

C - CYSTEAMIN ( BIOLOGICAL PRECURSOR OF COA) 750 MG I/V FOR 3 DOSES AT 1 - 3 DAYS INTERVALS.